Aryl hydrocarbon receptor/dioxin receptor in human monocytes and macrophages

[1]  Qiang Ma,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced Degradation of Aryl Hydrocarbon Receptor (AhR) by the Ubiquitin-Proteasome Pathway , 2000, The Journal of Biological Chemistry.

[2]  Y. Taketani,et al.  Expression of Ah receptor and dioxin-related genes in human uterine endometrium in women with or without endometriosis. , 1999, Endocrine journal.

[3]  R. Pollenz,et al.  Aryl Hydrocarbon Receptor Imported into the Nucleus following Ligand Binding Is Rapidly Degraded via the Cytosplasmic Proteasome following Nuclear Export* , 1999, The Journal of Biological Chemistry.

[4]  Ian L. Rogers,et al.  Resveratrol has antagonist activity on the aryl hydrocarbon receptor: implications for prevention of dioxin toxicity. , 1999, Molecular pharmacology.

[5]  S. Safe,et al.  Regulation of constitutive gene expression through interactions of Sp1 protein with the nuclear aryl hydrocarbon receptor complex. , 1999, Biochemistry.

[6]  H. Ciolino,et al.  Dietary flavonols quercetin and kaempferol are ligands of the aryl hydrocarbon receptor that affect CYP1A1 transcription differentially. , 1999, The Biochemical journal.

[7]  Jae-ho Yang,et al.  Expression of dioxin-responsive genes in human endometrial cells in culture. , 1999, Biochemical and biophysical research communications.

[8]  S. Dertinger,et al.  Flavone antagonists bind competitively with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) to the aryl hydrocarbon receptor but inhibit nuclear uptake and transformation. , 1999, Molecular pharmacology.

[9]  C. Tohyama,et al.  Cross-talk between 2,3,7,8-tetrachlorodibenzo-p-dioxin and testosterone signal transduction pathways in LNCaP prostate cancer cells. , 1999, Biochemical and biophysical research communications.

[10]  H. Ciolino,et al.  The flavonoid galangin is an inhibitor of CYP1A1 activity and an agonist/antagonist of the aryl hydrocarbon receptor , 1999, British Journal of Cancer.

[11]  M. Gallo,et al.  Ah Receptor and NF-κB Interactions, a Potential Mechanism for Dioxin Toxicity* , 1999, The Journal of Biological Chemistry.

[12]  M. Gallo,et al.  Ah receptor and NF-kappaB interactions, a potential mechanism for dioxin toxicity. , 1999, The Journal of biological chemistry.

[13]  Y. Fujii‐Kuriyama,et al.  Identification of a novel mechanism of regulation of Ah (dioxin) receptor function. , 1999, Genes & development.

[14]  D. Phelan,et al.  Activation of the Ah receptor signal transduction pathway by bilirubin and biliverdin. , 1998, Archives of biochemistry and biophysics.

[15]  D. Moore,et al.  Alternative Splicing Variants of IκBβ Establish Differential NF-κB Signal Responsiveness in Human Cells , 1998, Molecular and Cellular Biology.

[16]  S. Crews,et al.  Control of Cell Lineage-specific Development and Transcription by Bhlh–pas Proteins , 2022 .

[17]  A. Puga,et al.  Constitutive Activation of the Aromatic Hydrocarbon Receptor , 1998, Molecular and Cellular Biology.

[18]  N. Kaminski,et al.  Leukocyte activation induces aryl hydrocarbon receptor up-regulation, DNA binding, and increased Cyp1a1 expression in the absence of exogenous ligand. , 1997, Molecular pharmacology.

[19]  J. Sundberg,et al.  Lesions of Aryl-hydrocarbon Receptor–deficient Mice , 1997, Veterinary pathology.

[20]  Y Fujii-Kuriyama,et al.  CBP/p300 functions as a possible transcriptional coactivator of Ah receptor nuclear translocator (Arnt). , 1997, Journal of biochemistry.

[21]  J. Bend,et al.  Aryl hydrocarbon receptor-dependent induction of cyp1a1 by bilirubin in mouse hepatoma hepa 1c1c7 cells. , 1997, Molecular pharmacology.

[22]  D. Baden,et al.  Brevetoxin-6 (PbTx-6), a nonaromatic marine neurotoxin, is a ligand of the aryl hydrocarbon receptor. , 1997, Archives of biochemistry and biophysics.

[23]  T. Pineau,et al.  Ah receptor-dependent CYP1A induction by two carotenoids, canthaxanthin and beta-apo-8'-carotenal, with no affinity for the TCDD binding site. , 1997, Biochemical pharmacology.

[24]  D. Schrenk,et al.  Tryptanthrins: a novel class of agonists of the aryl hydrocarbon receptor. , 1997, Biochemical pharmacology.

[25]  S. Safe,et al.  Identification of a motif within the 5' regulatory region of pS2 which is responsible for AP-1 binding and TCDD-mediated suppression. , 1997, Biochemistry.

[26]  S. Lee,et al.  Murine Cyp1a-1 induction in mouse hepatoma Hepa-1C1C7 cells by myristicin. , 1997, Biochemical and biophysical research communications.

[27]  C. Bradfield,et al.  Ligand-dependent Interaction of the Aryl Hydrocarbon Receptor with a Novel Immunophilin Homolog in Vivo* , 1997, The Journal of Biological Chemistry.

[28]  J. P. Whitlock,et al.  A Novel Cytoplasmic Protein That Interacts with the Ah Receptor, Contains Tetratricopeptide Repeat Motifs, and Augments the Transcriptional Response to 2,3,7,8-Tetrachlorodibenzo-p-dioxin* , 1997, The Journal of Biological Chemistry.

[29]  Anita Nur Mayani,et al.  Dioxin concentrations in women with endometriosis. , 1997, Human reproduction.

[30]  J. Bend,et al.  Aryl Hydrocarbon Receptor-Dependent Induction of Cyp 1 a 1 by Bilirubin in Mouse Hepatoma Hepa 1 c 1 c 7 Cells , 1997 .

[31]  K. Umesono,et al.  Thioredoxin: a redox-regulating cellular cofactor for glucocorticoid hormone action. Cross talk between endocrine control of stress response and cellular antioxidant defense system. , 1996, The Journal of clinical investigation.

[32]  I. Kharat,et al.  Antiestrogenic Effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Are Mediated by Direct Transcriptional Interference with the Liganded Estrogen Receptor , 1996, The Journal of Biological Chemistry.

[33]  Y. Makino,et al.  Ligand-independent activation of the glucocorticoid receptor by ursodeoxycholic acid. Repression of IFN-gamma-induced MHC class II gene expression via a glucocorticoid receptor-dependent pathway. , 1996, Journal of immunology.

[34]  F. Askari,et al.  Hepatic fibrosis in Ahr-/- mice. , 1996, Science.

[35]  J. Bergman,et al.  Structure elucidation of two tryptophan-derived, high affinity Ah receptor ligands. , 1995, Chemistry & biology.

[36]  J. Bartholomew,et al.  Regulation of CYP1A1 by Indolo[3,2-b]carbazole in Murine Hepatoma Cells (*) , 1995, The Journal of Biological Chemistry.

[37]  Y. Honma,et al.  Expression of Ah receptor (TCDD receptor) during human monocytic differentiation. , 1995, Carcinogenesis.

[38]  T. Pineau,et al.  Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor , 1995, Science.

[39]  R. Stone Dioxin receptor knocked out , 1995, Science.

[40]  L. Poellinger,et al.  Agonistic and antagonistic effects of alpha-naphthoflavone on dioxin receptor function. Role of the basic region helix-loop-helix dioxin receptor partner factor Arnt. , 1994, The Journal of biological chemistry.

[41]  O. Gotoh,et al.  Interindividual difference in expression of human Ah receptor and related P450 genes. , 1994, Carcinogenesis.

[42]  S. Safe,et al.  Mechanism of 2,3,7,8-tetrachlorodibenzo-P-dioxin (TCDD)-mediated decrease of the nuclear estrogen receptor in MCF-7 human breast cancer cells , 1993, Molecular and Cellular Endocrinology.

[43]  L. Poellinger,et al.  Ligand-dependent recruitment of the Arnt coregulator determines DNA recognition by the dioxin receptor , 1993, Molecular and cellular biology.

[44]  L. Poellinger,et al.  Nonresponsiveness of normal human fibroblasts to dioxin correlates with the presence of a constitutive xenobiotic response element-binding factor. , 1993, The Journal of biological chemistry.

[45]  S. Safe,et al.  alpha-Naphthoflavone-induced CYP1A1 gene expression and cytosolic aryl hydrocarbon receptor transformation. , 1993, Molecular pharmacology.

[46]  O. Hankinson,et al.  Identification of the Ah Receptor Nuclear Translocator Protein (Arnt) as a Component of the DNA Binding Form of the Ah Receptor , 1992, Science.

[47]  S. Safe,et al.  Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on cell growth and the secretion of the estrogen-induced 34-, 52- and 160-kDa proteins in human breast cancer cells , 1990, The Journal of Steroid Biochemistry and Molecular Biology.

[48]  J. Gierthy,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin causes an extensive alteration of 17 beta-estradiol metabolism in MCF-7 breast tumor cells. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[49]  S. Safe,et al.  Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds on the occupied nuclear estrogen receptor in MCF-7 human breast cancer cells. , 1990, Cancer research.

[50]  S. Safe,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin as an antiestrogen: effect on rat uterine peroxidase activity. , 1990, Biochemical pharmacology.

[51]  J. Gustafsson,et al.  The specific DNA binding activity of the dioxin receptor is modulated by the 90 kd heat shock protein. , 1990, The EMBO journal.

[52]  J. Gustafsson,et al.  Specific protein-DNA interactions at a xenobiotic-responsive element: copurification of dioxin receptor and DNA-binding activity. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[53]  J. Mathis,et al.  Identification of multiple regulatory elements on the human cytochrome P450IA1 gene. , 1988, Carcinogenesis.

[54]  M. Romkes,et al.  Comparative activities of 2,3,7,8-tetrachlorodibenzo-p-dioxin and progesterone as antiestrogens in the female rat uterus. , 1988, Toxicology and applied pharmacology.

[55]  Y. Fujii‐Kuriyama,et al.  Characterization of xenobiotic responsive elements upstream from the drug-metabolizing cytochrome P-450c gene: a similarity to glucocorticoid regulatory elements. , 1987, Nucleic acids research.

[56]  E. Unanue,et al.  The basis for the immunoregulatory role of macrophages and other accessory cells. , 1987, Science.

[57]  P. Chomczyński,et al.  Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. , 1987, Analytical biochemistry.

[58]  O. Hankinson,et al.  Intracellular location of the Ah receptor , 1986, Journal of cellular physiology.

[59]  J. Whitlock,et al.  Control of cytochrome P1-450 gene expression: analysis of a dioxin-responsive enhancer system. , 1986, Proceedings of the National Academy of Sciences of the United States of America.

[60]  J. Whitlock,et al.  Control of cytochrome P1-450 gene expression by dioxin. , 1985, Science.

[61]  C. Wade,et al.  Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. , 1978, Toxicology and applied pharmacology.

[62]  U. K. Laemmli,et al.  Cleavage of structural proteins during , 1970 .